Publication | Open Access

Functional alterations in gap junction channels formed by mutant forms of connexin 32: evidence for loss of function as a pathogenic mechanism in the X-linked form of Charcot-Marie-Tooth disease

Gap Junction ChannelsConnexin 32Signal TransductionMolecular PhysiologyCharcot-marie-tooth DiseasePathogenesisMolecular BiologyIntercellular CommunicationCell JunctionsMedicineCell BiologyCell SignalingCellular Physiology